ABSTRACT
This chapter explores the evidence and rationale forming the hypothesis that oxidative stress underlies the neuropathogenesis of organomercurials. Since methylmercury (MeHg) is one of the most common and most toxic environmental forms of mercury, the majority of experimental studies have focused on this agent. The chapter addresses many organomercurials that share properties with MeHg, other compounds. Notably, a small percentage of organic mercury accumulated in brain tissue is converted to inorganic mercury. The chapter includes oxidative stress caused by inorganic mercury. It considers strategies for the rationally directed engineering of cells to confer protection against MeHg. Mitochondria are dependent on several sulfhydryl-dependent proteins for normal function and are implicated in the regulation of programmed cell death. Glutathione serves as a primary line of cellular defense against mercury compounds. MeHg has been demonstrated to increase phospholipase activity in cultures of cerebellar granule neurons and in liposomes.
